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Circulating Transforming Growth Factor-β1*: A Potential Marker of Disease Activity During Idiopathic Pulmonary Fibrosis

Suk-Joong Yong, MD, PhD; Arun Adlakha, MD, FCCP; Andrew H. Limper, MD, FCCP
Author and Funding Information

*From the Division of Pulmonology (Dr. Yong), Wonju Medical College, Yonsei University, Wonju, Korea; Carolina Respiratory Specialists (Dr. Adlakha), Charlotte, NC; and the Thoracic Diseases Research Unit (Dr. Limper), Division of Pulmonary Critical Care and Internal Medicine, Mayo Clinic, Rochester, MN.

Correspondence to: Andrew H. Limper, MD, PhD, Thoracic Diseases Research Unit, 601C Guggenheim Building, Mayo Clinic, Rochester, MN 55905; e-mail: limper.andrew@mayo.edu



Chest. 2001;120(1_suppl):S68-S70. doi:10.1378/chest.120.1_suppl.S68
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Extract

Idiopathic pulmonary fibrosis (IPF) is characterized by patchy inflammatory infiltration of the lungs with mesenchymal cell proliferation, extracellular matrix deposition, and progressive loss of normal lung architecture. Active lesions of IPF are comprised of macrophage-rich fibrinous alveolar exudates in regions of epithelial injury. These exudates subsequently organize by fibroblast infiltration and deposition of extracellular matrix proteins including fibronectins, collagens, and proteoglycans, which generate the active fibroblastic foci typical of IPF. Prior work by our group and others has strongly implicated transforming growth factor (TGF)-β1 in promoting fibroblastic proliferation and matrix accumulation in fibrotic lung diseases.13 Inhibition of TGF-β has recently been proposed as a potential therapeutic avenue for the management of lung fibrosis.4

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